The mice lost a little weight from the stress, but not more than they did from just eating a fatty diet — so the plaque bursts weren’t caused by extreme sickness or starvation.

Scientific Claim

In apolipoprotein E-knockout mice, the combination of high-fat diet, carotid collar placement, and short-term stress (LPS, phenylephrine, cold) induces plaque rupture without altering body weight significantly beyond the effect of diet alone, indicating that the rupture model is not confounded by extreme metabolic stress.

Original Statement

“Body weight was lower in the treatment group than in the control groups at both time points (P<0.05).”

From study:Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Evidence Quality Assessment

Claim Status

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

association

Can only show association/correlation

Assessment Explanation

The study reports body weight changes as a secondary observation and does not overinterpret them. The association is appropriately framed as a non-confounding factor.

Evidence from Studies

Supporting (1)

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Cohort Study

Animal

2013 Jul

Scientists made mice with artery plaques get stressed in short bursts (like being cold or injected with a stress chemical), and the plaques broke open — but the mice didn’t get much heavier than they already were from eating fatty food. This means the breaking wasn’t just because they were super obese.

Contradicting (0)

No contradicting evidence found

Source Study

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Score: 17

DOI: 10.1038/cmi.2013.4

Similar Assertions

In mice with fatty artery buildup, a quick burst of stress (like cold, a toxin, and a blood pressure drug) caused 3 out of 4 fragile plaques to burst, but only if the plaque was already weak — strong plaques didn’t break.

89%

Even though the mice had fatty plaques and they burst, their blood fat levels didn’t change — meaning the rupture wasn’t caused by worse cholesterol, but by something else, like immune activity.

75%

The mice didn’t gain or lose weight or eat differently with the drug, so the benefits aren’t just because they were eating less or changing their metabolism.

73%

The drug didn’t affect blood sugar or fat levels in the blood, so its benefits aren’t due to improving how the body handles sugar or fat.

72%

The drug didn’t lower the mice’s overall cholesterol, so its benefits must come from something else—like reducing inflammation or cell death in plaques.

71%